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Paris, 24 November 2015
Press release
A new neural circuit involved in the control of movement
The team led by Claire Wyart, an Inserm researcher at the Brain and Spine
Institute, has just demonstrated the ability of sensory neurons located in the
spinal cord to modulate movement. In the zebrafish, the researchers have
shown that activation of these neurons triggers locomotion when the animal is
at rest, and inhibits it when the animal is moving. These results offer hope that
it will one day be possible to specifically stimulate these circuits in order to
generate movement in patients with spinal cord injuries. This work is
published in Current Biology.
Spinal cord injuries lead to serious paralysis for which, to date, there is no treatment. When
communication between the brain and spinal cord is interrupted, the brain can no longer control
movements voluntarily. However, the spinal cord contains autonomous circuits that generate
movement, and ensure that locomotion proceeds once the decision to move has been taken at brain
level. This capacity for sustaining movement comes from the ability of the spinal locomotor network to
generate electrical oscillations.
In order to understand the functioning and modulation of the spinal locomotor network, Claire Wyart’s
team studies motor activity in the zebrafish. This transparent vertebrate species is particularly suited
to optogenetics, an innovative technology that allows stimulation of target neurons using light. In this
method, the stimulated neurons light up and are visible in the transparent animal.
The researchers exploited this technology to identify and understand the functioning of a new neural
circuit involved in the control of movement. By activating the circuit at different times (animal at rest or
moving), the researchers demonstrated connections that can generate the oscillations that allow the
fish to move. The originality of this circuit is that it depends on the activity of sensory neurons, which,
through a cascade effect, ultimately activate motor neurons.
Surprisingly, the researchers find that modulation of movement depends on the animal’s initial state.
In fact, stimulation triggers movement when the animal is in a resting state, whereas it inhibits it when
the animal is already swimming. “This modulation is complex, and will depend on the context,”
explains Claire Wyart, the main author of this work.
In 2014, this same team had shown that this circuit is conserved among the different vertebrate
species, particularly in primates. This original work in the zebrafish thus opens many avenues of
research for understanding the modulation of the locomotor circuit in humans.
For the first time, a class of sensory neurons that can modulate the spinal locomotor network has
been identified. Although several points remain to be clarified, stimulation of the sensory pathways to
activate the locomotor network that generates walking in humans represents hope in cases of spinal
cord injury.
Brain stem
Spinal cord
Rostral
spinal cord
Caudal
spinal cord
Dorsal view of the spinal cord in the zebrafish at 4 days of development. Illustration of the
movement-modulating spinal circuit according to the animal’s locomotor context.
In red: interneurons known as “excitatory” involved in the control of movement
In green: GABAergic sensory neurons that are “inhibitory” on contact with the cerebrospinal fluid.
Source
State-dependent modulation of locomotion by GABAergic spinal sensory neurons
Kevin Fidelin1,2,3,4, Lydia Djenoune1,2,3,4,5, Caleb Stokes1,2,3,4, Andrew Prendergast1,2,3,4,
Johanna Gomez1,2,3,4, Audrey Baradel1,2,3,4, Filippo Del Bene4,6 and Claire Wyart1,2,3,4,*
1Brain and Spine Institute (ICM), F-75013, Paris, France
2INSERM UMRS 1127
3French National Centre for Scientific Research (CNRS) UMR 7225
2UPMC – University of Paris 6, F-75005, Paris, France.
5National Museum of Natural History, F-75005, Paris, France
6Institut Curie, CNRS UMR 3215, INSERM U934, F-75005, Paris, France
Current Biology.
Investigator contact
Claire Wyart
Inserm Unit 1127, “Brain and Spine Institute”
Tel. +33 (0)1 57 27 43 10
[email protected]
Press contact
[email protected]
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